Matsuda O, Nonoguchi H, Tomita K, Shiigai T, Ida T, Shinohara S, Ideura T, Takeuchi J
Second Department of Internal Medicine, Tokyo Medical and Dental University, Yushima, Japan.
Nephron. 1988;49(3):203-9. doi: 10.1159/000185056.
A 65-year-old woman with mild renal insufficiency had persistent hyperkalemia and hyperchloremic acidosis. Her plasma aldosterone level was relatively low for her hyperkalemia, and her urine pH was low. Fludrocortisone acetate administration corrected both hyperkalemia and acidosis by increasing urinary excretion of potassium and net acid, implicating deficient mineralocorticoid activity in the distal renal tubule in this patient. During this medication urinary ammonium excretion increased, but urine pH remained low, so that urinary titratable acid excretion did not decrease. On the other hand, correction of hyperkalemia by administration of a potassium-calcium exchange resin alone also resolved the acidosis by increasing urinary ammonium excretion. This increment exceeded the decrement of urinary titratable acid excretion, which was caused by raised urine pH secondary to increased urinary ammonium excretion, and resulted in increase of net acid excretion. Thus, in this patient, hyperkalemia appears to be a decisive causative factor in the acidosis, with deficient mineralocorticoid effect only contributing in part to the reduction of net acid excretion and the acidosis.
一名65岁轻度肾功能不全女性患有持续性高钾血症和高氯性酸中毒。对于她的高钾血症而言，其血浆醛固酮水平相对较低，且尿液pH值较低。给予醋酸氟氢可的松通过增加尿钾排泄和净酸排泄纠正了高钾血症和酸中毒，提示该患者远端肾小管盐皮质激素活性不足。在用药期间，尿铵排泄增加，但尿液pH值仍低，因此尿可滴定酸排泄未减少。另一方面，单独给予钾钙交换树脂纠正高钾血症也通过增加尿铵排泄解决了酸中毒。这一增加超过了因尿铵排泄增加导致尿液pH值升高而引起的尿可滴定酸排泄的减少，并导致净酸排泄增加。因此，在该患者中，高钾血症似乎是酸中毒的决定性致病因素，盐皮质激素作用不足仅部分导致净酸排泄减少和酸中毒。
